For thousands of years, people have practiced meditation for spiritual awakening and awareness, but that is not meditation’s only benefit. Studies show that it helps to deepen sleep, even in people who do not have sleep issues.
Fortunately, meditating is free, and it doesn’t require equipment. You can also do it nearly anywhere.
How Does Meditation Help Me to Sleep?
Whether you have regular insomnia or you just need some help adjusting to a new sleep schedule, meditation before sleep may have benefits. Researchers have a few theories about why meditation may help you sleep better:
Pain reduction. Meditating may reduce pain. A preliminary study showed that meditation helps with pain relief without engaging the brain’s naturally occurring opioid chemicals.
Another study on people with fibromyalgia, a chronic pain condition, showed that meditation reduced their anger and worry about their condition.
If chronic pain keeps you awake at night, developing a meditation practice can help.
Mental health. Doing meditation for insomnia can relieve anxiety, depression, and stress, helping you to sleep better. A review of over 200 studies showed that meditation can have a positive effect on mental health.
Preparing the body for sleep. Meditation slows down your heart rate and lowers the levels of the stress hormone cortisol in your body, two things that happen naturally when you sleep. Meditation can also cause you to have theta brainwaves, the same state your brain enters when you are falling asleep.
How Do I Meditate Before Sleep?
When you prepare to meditate, make sure that you are in a comfortable position and that you are unlikely to be disturbed. Put your phone on silent and turn off the TV.
There are many ways to meditate. You can do it however you’d like. When most people meditate, they sit comfortably or lie down, close their eyes, and try to clear their minds. If you are having trouble getting started, look for meditation classes or join a local group meditation.
There’s no set amount of time required to meditate. You can try it for just a few minutes, or do it for an hour. However, research does show that meditating for between 10 and 30 minutes may be more effective for helping sleep.
Meditation is all about letting go of judgment. Thoughts may come into your head as you try to relax. Simply observe them without judgment. Notice them, and allow them to fade away as you focus on your meditation.
There are many ways you can meditate for sleep including:
Box breathing. While lying down, breathe in for a count of four. Then breathe out while counting to four again.
Guided meditations. There are apps for your phone and videos online that offer guided meditations. These recordings are on different topics and use different techniques. Find one that you like and give it a try.
Calming sounds. Some people enjoy meditating while listening to calming music or natural sounds like rain or ocean waves.
Body scan meditation. Without moving or opening your eyes, focus on your toes. Notice how they feel before moving up to the next body part. Continue doing this until you’ve done your whole body up to your fingertips and top of your head.
Body relaxation meditation. This is very similar to a body scan meditation. Starting at your toes, notice how they feel. Then tense them up. Finally, relax them as much as you can. Do the same for your whole body.
Does Meditation Have Health Risks?
Meditation is considered to be very safe. However, you should talk to your doctor before beginning a meditation practice if you have a history of mental illness. In rare cases, meditation can worsen your symptoms.
Meditation should not be used in place of medical care. If you have serious insomnia, you can try meditation to help, but you should also talk to your doctor about other things that might help you sleep better.
Meditation doesn’t work for everyone to improve sleep. There are also many meditation types. So, it may take some trial and error to find the one that works for you.
Some traits you were born with — your eye color and hair color, for example — come from your genes. They’re molecules – scientists need a microscope to see them — that carry information passed down from your parents. It’s called DNA, and most is the same for everybody. But a small percentage of it is yours alone. Those differences help determine how you look, the way your body works, your risk for diseases, and your personality.
Sunlight Sneeze
2/13
Have you ever noticed that you feel the urge to sneeze when you step into bright light? It’s called photic sneeze reflex, and it seems to happen in about a quarter of the population. It’s not clear just how light can lead to sneezing, but scientists do know that it’s tied to a gene your parents pass down to you. If one parent is a sun-sneezer, their child has a 50% chance of being one, too.
Perfect Pitch
3/13
A trained musician can typically sing you a note, like a G, as long as you give them a “starting pitch,” like C, and say what it is. That’s relative pitch. If you have absolute, or perfect, pitch, you can hear or sing any note without hearing another one first. Your genes might play a part in this skill. In a survey, people with perfect pitch were more likely to have a close relative who had it. Still, musical training makes a difference.
Earwax
4/13
Is yours dry, grayish, and flaky? Or wet, yellow, and sticky? It depends on which version, or allele, you have of one gene, called ABCC11. The same gene is tied to the smell of the sweat in your armpits as well. If you have the allele for wet, sticky earwax, you’re more likely to have body odor than someone with the other kind.
Lark or Owl?
5/13
The time of day when you’re most alert and productive is driven by your body’s internal clock, or circadian rhythm. Most people’s run on about a 24-hour schedule, but it can run faster or slower, making you a morning lark or a night owl. Specific genes seem to play a role in your circadian rhythm speed and how closely it matches the 24-hour day. Changes in those genes can cause disorders that make you fall asleep and wake up at odd hours.
The Roots of Gray Hair
6/13
We all wonder when we’ll get our first gray strand. Scientists found a gene that helps figure out if — and how early — you’ll get yours. The gene, called IRF4, helps make the pigment in your hair, eyes, and skin. It may give us insight on aging and possibly how to hold off those silver locks.
Researchers also found genes linked to balding, curly hair, and unibrow.
Your Father’s Influence
7/13
You know that a pregnant woman’s age, diet, weight, and other habits can affect their baby’s health. But do you know the same is true for the father?
As men get older, if they gain a lot of weight or become heavy drinkers, their genes can change. If passed down, those changes may raise their kids’ — or even grandkids’ — chances of getting conditions like autism, diabetes, and cancer.
Weight in Your Genes
8/13
What you eat and how much you exercise isn’t the whole story when it comes to your size. Your DNA also may play a part. Scientists have found that some people’s genes nudge them toward a higher-than-healthy weight. A nutritious diet tips the scales in your favor.
A Better Look at Blindness
9/13
Experts now believe several dozen gene variations may raise the risk of age-related macular degeneration (AMD). It’s the leading cause of blindness in people 50 and older.
Some combinations have been tied to wet AMD, a more advanced form of the disease.
This means doctors may one day be able to test for genetic risk and come up with new ways to prevent or treat both disorders.
Gluten Glitch
10/13
About 40% of us might have genes linked to celiac disease. That’s the disorder that stops you from digesting gluten and causes inflammation in the intestines. But only about 1% of the people with these genes have symptoms of the disease. Scientists aren’t sure what makes the difference.
Viruses That Boost Immunity
11/13
Our ancestors faced many viral illnesses as our species evolved.
Today, a bit of your DNA is made of leftovers from the viruses our ancestors fought off. Scientists used to think these strange bits had no purpose. But when they removed them from cells in a lab, other nearby genes were no longer able to trigger the immune system to fight off new virus attacks.
As it turns out, those ancient viruses have been protecting us against new ones.
Meet Your Cousin, the Worm
12/13
Researchers in Japan say people share about 14,000 genes — or roughly 70% of their genetic makeup — with tiny acorn worms. These creatures live in the water and breathe through slits in their guts similar to fish gills. There’s evidence those slits evolved into our jaw, tongue, voice box, and throat muscles.
It’s Nature AND Nurture
13/13
If all this makes you wonder about what could be hiding in your DNA, remember this: Your health, personality, and looks are based on many things, including your genes. Your environment, lifestyle, and a bit of chance also make a difference.
The choices you make still matter most as far as who you’ll become, though.
Editor’s note: A version of this article was originally published on Jennifer Margulis’s Substack channel, Vibrant Life. Support independent journalism by subscribing to her channel.
Our friend and colleague, J.B. Handley, a graduate of Stanford University, a successful investor, and a father of three, has a young adult son with nonverbal autism.
As he details in his book, How to End the Autism Epidemic, Handley–like literally hundreds of thousands of other parents (including this one, this one, this one, this one, and this one)–watched firsthand how the vaccines given to his boy at every “well baby” visit caused his son Jamison to slip away into autism.
At the same time, the connection between vaccines and autism has been soundly dismissed by the CDC and the vaccine manufacturers. They insist that vaccines are “safe and effective” and that the idea that vaccines may cause autism–or any other health issue, for that matter–is nothing but “conspiracy theory.”
This blanket dismissal is nonsensical. Many excellent books have been written about why. For those of you who are new to thinking about vaccine safety issues, I’ll give you a few highlights.
Every vaccine has a different safety and efficacy profile. To say “vaccines are safe and effective” is akin to saying: “Gas works and all gas works for every car.” Then, when a car that takes diesel runs rough on unleaded fuel, you blame everything but the gasoline.
The CDC continues to add vaccines to the schedule without removing any. While any given vaccine may be safe (see #1), overloading a child’s body with so many vaccines so soon is not.
Autism is likely multifactorial. There may be several environmental toxins that cause autism. At the same time, there are now hundreds of studies that show that children who receive fewer vaccines or none at all have a lower risk of many health problems, including autism and other forms of brain damage, infant mortality, and several chronic illnesses, including asthma, central nervous system demyelinating syndromes, and chronic arthritis.
Not a Conspiracy Theory
Despite the pharmaceutically-funded pseudo-science that claims otherwise, over-vaccination is likely a causative if not the causative factor in the rise in autism in the United States. In other words, yes, vaccines cause autism.
The truth is that our autism rates should be 1 in 10,000, which is what they were in the 1970s. Which implies that the vast majority of cases of severe autism can be prevented. There are safe and effective ways to help prevent your child from suffering from toxicant-induced brain and immunological damage. There are also safe and effective ways to recover your child from environmentally induced autism.
Some Backstory
In the late 1990s in the United States, the U.S. Food and Drug Administration began calculating the amount of mercury infants were receiving via intramuscular injection courtesy of childhood vaccines.
At that time, mercury, in the form of thimerosal, was added to vaccines as a preservative. But since in the United States, vaccines are approved on a vaccine-by-vaccine basis, no government agency had ever calculated the cumulative amounts of mercury exposure American babies were being subjected to.
The math yielded worrisome results. Government officials realized that the amount of mercury the average child was receiving far exceeded maximum safety levels. As David Kirby details in his 2005 bestseller, Evidence of Harm: Mercury in Vaccines and the Autism Epidemic: A Medical Controversy, many parents believed that their children with autism were exhibiting symptoms of mercury poisoning.
To test whether the mercury in vaccines was causing brain damage, the CDC commissioned Thomas Verstraeten, M.D., to compare health outcomes in children who had received high doses of mercury early in their lives with children who hadn’t received any mercury.
When he crunched the numbers, Verstraeten found large statistically significant correlations between high doses of mercury and outcomes like autism, ADHD, tics, and speech disorders. He redid the numbers the next month and found an even higher correlation for autism. In fact, autism was more than 11 times as common in the high early exposure group than the non-exposure group.
These first calculations were nicknamed “Generation Zero” by the people at SafeMinds, a non-profit organization dedicated to ending the autism epidemic by supporting environmental research and effective treatments. SafeMinds, which was co-founded by Sallie Bernard and Lyn Redwood (a nurse married to a medical doctor), received the information through a Freedom of Information Act request.
So what did the CDC do with that information? First, they tried to make the signal go away. Then, when they couldn’t, they called a closed-doors secret meeting in June of 2000 at the Simpsonwood Retreat Center in Norcross, Georgia, to which they also invited vaccine manufacturers.
One doctor at that meeting insisted he didn’t want his new grandson to be injected with any thimerosal-containing vaccines. But, true to form, the Simpsonwood participants still managed to convince themselves there was nothing to worry about.
In fact, what they were most concerned about was the damage this information could do to the overall childhood vaccine program, not the damage that the vaccines were actually doing to the brains and bodies of America’s children. So, presumably with clear consciences, they decided not to make any of the worrisome findings available to the public.
Verstraeten massaged the numbers a few more times. Three years after the secret meeting at Simpsonwood, he finally managed to make enough of the signal go away that what remained was statistically insignificant–except for the connection between mercury-containing vaccines and tics. The end result was a neutral study, published in the peer-reviewed journal Pediatrics in 2003, with no consistent findings. The authors reported “conflicting results” and could not make any definitive statements or reach any conclusions about whether thimerosal in vaccines caused brain damage.
The data was so inconclusive and the water so muddy, in fact, that all the scientists concluded was: “For resolving the conflicting findings, studies with uniform neurodevelopmental assessments of children with a range of cumulative thimerosal exposures are needed.”
But that wasn’t how the press reported it. Verstraeten’s “neutral” study was touted as “proof” that vaccines didn’t cause autism, even though the good folks at the CDC knew that it was anything but.
Without ever admitting a causal link between thimerosal and brain damage, vaccine manufacturers began a voluntary phase-out of mercury in vaccines.
While mercury is now used as an ingredient in only three brands of vaccines for influenza as well as one brand of tetanus-diphtheria vaccine, the problem of environmentally-induced autism continues.
Our public health officials continue turning a blind eye to the damages caused by the cumulative exposure to harmful vaccine ingredients.
Many of the world’s experts on aluminum–a known neurotoxin which is present in many of the childhood vaccines as an adjuvant–believe this ingredient is also causing brain damage and immunological damage to children born today.
One such expert is Dr. Christopher Exley, author of the book, Imagine You Are an Aluminum Atom. In a 2017 study, Exley and his team found high levels of aluminum in the brain tissue of autistic subjects. The sample study was small but the findings were significant. The location of this stored aluminum, inside inflammatory cells in brain tissue, led the researchers to speculate that aluminum could penetrate the blood–brain barrier through these inflammatory cells from a vaccine injection site.
These findings, however, did not seem to interest or concern public health officials. The response, as expected, has been to simply declare aluminum-adjuvant containing vaccines “safe.”
His research on aluminum in vaccines has had repercussions for Exley’s career, however. First, Keele University stopped sending press releases about his work. Then they silenced him and stopped his research by forbidding him from accepting any outside funding and shutting down his website, thus forcing him out of his job.
What About the MMR Vaccine and Autism?
If vaccines didn’t cause autism, we would no longer be talking about this issue. But hundreds of thousands of parents continue to witness severe health declines in their children after following their mainstream doctors’ orders. In the late 1990s, a group of these parents begged British gastroenterologists to help them.
A group of Britain’s best medical doctors at the Royal Free Hospital in London teamed up to figure out what was going on with these children.
Their extensive research led to the publication of a now infamous scientific paper whose lead author was a young gastroenterologist named Andrew Wakefield.
The now-retractedscientific paper mentioned that parents of children suffering from regressive brain disorders along with unusual intestinal problems reported that both conditions began shortly after their children received the live virus MMR vaccine (given to children to help protect them against measles, mumps, and rubella).
The MMR vaccine is a live-virus vaccine. It has never contained thimerosal or aluminum.
Vaccine apologists have criticized vaccine safety advocates for investigating different vaccines and analyzing the toxicity of different ingredients in their quest to better understand vaccine-induced brain damage.
Apologists complain that this is “moving the bar.” But the truth is autism rates keep going up and parents continue to report severe immune, gastrointestinal, and cerebral damage after vaccines. That is a clinical signal that should be investigated–not dismissed or ignored.
We can’t blame Andrew Wakefield or Jenny McCarthy. Most of today’s young parents have no idea who they are. Vaccine hesitancy does not continue because of an obscure now retracted paper published by a team of 13 scientists and retracted over a decade later.
No, vaccine hesitancy continues because parents continue to see poor health outcomes post-vaccination.
Vaccine apologists should be the most eager to champion and fund more vaccine safety research. Since they are sure that vaccines don’t cause autism, this research should exonerate vaccines once and for all.
The truth is we cannot say vaccines don’t cause autism until we have investigated every ingredient and every vaccine, as well as the potential for synergistic toxic effects of so many vaccines given to such young children.
It may be that the timing of the MMR vaccine–usually given between twelve and fifteen months–coincides coincidentally with the onset of autism symptoms, as some vaccine apologists have argued.
But it is also possible that the strong immune response provoked by the MMR vaccine plays a causative role in disrupting the brain.
The only accurate thing we can say about the connection between the MMR vaccines and autism is that parents have noticed a temporal association that scientists have not been able to adequately explain.
More Malfeasance at the CDC
A group of CDC researchers sought to get to the bottom of the MMR autism connection. They wanted to avoid the “irregularities” associated with the Verstraeten study by setting out a rigid protocol ahead of time. The problem was that when they did the study, they found that African-American boys who received the MMR “on time” (that is, before 36 months) were three and a half times more likely to develop autism than African-American boys who got the MMR vaccine after 36 months of age.
What did the CDC do this time? As Del Bigtree shows in his film, “Vaxxed: From Cover-up to Catastrophe,” instead of publishing the data, the CDC again massaged it. They changed the study’s protocol. They dropped subjects who didn’t have Georgia birth certificates.
Since parents had to pay for those birth certificates, the children who were dropped were generally from poorer families who were disproportionately African-American. This change in the study protocol allowed the researchers to dump 40% of their data showing the connection between early vaccination with MMR and autism in African-American boys. Once again, the signal almost went away. And, again, the pharmaceutical-funded mainstream media jumped on the published study to crow that it proved that the MMR vaccine does not cause autism.
A Whistleblower Comes Forward
But there was a glitch. One senior scientist at the CDC, William Thompson, Ph.D., who participated in manipulating the study’s data in order to hide the clear connection between the MMR vaccine and autism felt guilty about what he and his colleagues had done.
He reached out to Brian Hooker, Ph.D., a Professor of Biology at Simpson University in Redding, California, who is also a data analyst and autism dad, to assuage that guilt. Hooker recorded their phone conversations. What Thompson told Hooker was documented in the 2016 film “Vaxxed: From Cover-up to Catastrophe.”
The deliberate malfeasance in order to cover up the connection between vaccines and autism is devastating.
Given the CDC’s history of obfuscation on this subject, it shouldn’t be surprising that they utterly refuse to do the one type of study that could potentially settle the question forever: comparing health outcomes of a large number of randomly selected children who are fully vaccinated with the health outcomes of a large number of children who have never been vaccinated.
Every small study done to date has shown that unvaccinated children have less autism and enjoy better health than vaccinated children, as Dr. William Gaunt discusses in this article and this one. When Dr. Paul Thomas, M.D., hired an independent medical researcher to analyze the data in his practice, they found that children born into his practice who were exposed to the least amount of aluminum and the fewest vaccines also had the best health outcomes. However, this information is so threatening to the status quo that one of Dr. Paul’s two peer-reviewed scientific studies was retracted.
Retraction is an effective way to silence and discredit independent researchers whose publications threaten Big Medicine. Like data massage, it is a tool wielded by the pharmaceutical industry and the government entities they fund to keep information from you that they don’t want you to know.
It is imperative for the medical industrial complex to keep parents from knowing the truth about vaccine safety. The pharmaceutical industry and the American public “health” program that receives millions of dollars in funding from the pharmaceutical industry has too much to lose if the word gets out.
Are vaccines the sole cause of autism? No. Are there several other environmental factors that may be contributing to brain damage among America’s children, perhaps including over-exposure to ultrasound and over-exposure to toxic herbicides like glyphosate? Yes. Are some cases of autism simply genetic? Of course.
But there is no question that the CDC, the Department of Health and Human Services, and the vaccine manufacturers have colluded–and continue to collude–to hide data that indicate that vaccines can and do cause autism.
Pulse oximeters and other devices to monitor aspects of our health may work better for some than for others.
In recent years, there’s been a veritable explosion in the number and type of health monitoring devices available in smartphones and fitness apps.
Your smartphone is likely tracking the number of steps you take, how far and fast you walk, and how many flights of stairs you climb each day. Some phones log sleep, heart rate, how much energy you’re burning, and even “gait health” (how often are both feet on the ground? how even are your steps?). And, of course, nonphone wearables and fitness gadgets are available, such as devices to measure your heart rhythm, blood pressure, or oxygen levels. The accuracy of these devices varies — and, in some instances, your skin tone may make a difference.
Generally, how accurate are health monitors?
I know from my experience with hospital monitoring devices that they aren’t always accurate. False alarms from EKG monitors often send medical staff scurrying into patient rooms, only to find the patient feeling fine and surprised about the commotion. A particularly common false alarm is a dangerous and unstable heart rhythm on a continuous heart monitor, which can be due to the motion from a patient brushing their teeth.
High-stakes devices with monitoring capability, such as defibrillators and pacemakers, are extensively tested by their makers and vetted by the FDA, so their accuracy and reliability are generally quite good.
But what about home health monitoring devices intended for consumer use that are not extensively tested by the FDA? Ever count your steps for a few minutes just to see if your phone’s tally agrees? Or climb a couple of flights of stairs to see if you are getting full credit for not taking the elevator?
The accuracy of consumer devices depends in part on what is being monitored. For example, one study assessed the accuracy of heart rate monitors and energy expenditure calculators in phones and health apps. Accuracy was quite high for heart rate (often in the range of 95%), but much less accurate for energy expenditure. Accuracy can also vary depending on who is being monitored.
Device bias: What it is and why it occurs
While no health gadget is perfect, some users get more reliable results than others. For example, if you’re wearing nail polish, a pulse oximeter — a device that clips onto the fingertip to measure blood oxygen through the skin — may not work well, because the polish interferes with proper function of the light sensor. In that situation, there’s a simple solution: remove the polish.
But in other cases, the solution isn’t simple. Increasingly, we’re recognizing that certain medical devices are less accurate depending on a person’s skin color, a phenomenon called device bias.
Pulse oximeters. Although generally considered highly accurate and commonly relied upon in healthcare settings, their accuracy tends to be lower in people of color. That’s because the device relies on shining light through the skin to detect the color of blood, which varies by oxygen level. The amount of pigment in the skin may alter the way light behaves as it travels to blood vessels, leading to inaccurate results.
Bilirubin measurement in newborns. Bilirubin is a breakdown product of red blood cells. Newborns are screened for high levels because this can cause permanent brain damage. When detected, phototherapy (light treatments) can help the baby get rid of the excess bilirubin, preventing brain damage. The screening involves examining a newborn’s skin and eyes for jaundice (a yellowing due to elevated bilirubin), and a light meter test to detect high bilirubin levels. But the accuracy of this test is lower in Black newborns. This is particularly important because jaundice is more difficult to detect in infants with darker skin, and dangerously high bilirubin levels are more common in this population.
Heart rate monitors in smartphones. According to at least one study, smartphone apps may also be less accurate in people of color. Again, this is because the more skin pigment present, the more trouble light sensors have detecting pulsations in blood flow that reflect heartbeats.
Why device bias matters
Sometimes an error in measurement has no immediate health consequences. A 5% to 10% error rate when measuring heart rate may be of little consequence. (In fact, one could ask why anyone needs a device to monitor heart rate when you could just count your pulse for 15 seconds and multiply by 4!)
But pulse oximeter readings are used to help decide whether a person needs to be hospitalized, who requires admission to the intensive care unit, and who requires additional testing. If the oxygen level is consistently overestimated in people of color, they may be more likely to be undertreated compared with others whose readings are more accurate. And that may worsen previously existing healthcare disparities.
These examples add to the growing list of bias imbedded within healthcare, and other instances where failing to include diverse individuals has serious consequences. When you use a health device, it’s reasonable to wonder if it’s been tested on people like you. It’s also reasonable to expect people who develop medical and consumer health devices to widen the demographics of test subjects, to make sure results are reliable for all users before putting them on the market.
Sometimes a change in technology, such as using a different type of light sensor, can make health-related devices work more accurately for a wider range of people.
Or there may be no easy fix, and user characteristics will need to be incorporated into proper interpretation of the results. For example, a device could offer the user a choice of skin tones to match skin color. Then based on extensive data from prior testing of people with different skin colors, the device could adjust results appropriately.
The bottom line
The push to monitor our bodies, our health, and our life experiences continues to gain momentum. So we need to thoroughly test and validate health-related devices to be sure they work for diverse individuals before declaring them fit for the general public. An expert panel at the FDA has advocated for better regulation and testing of pulse oximeters to ensure they are accurate for all.
With even the best testing, device bias may not disappear: bodies vary, and technology has its limits. The key is to know it exists, fix what can be fixed, and interpret the results accordingly.
How will we know when it ends — and does it matter?
It seems like a long time since the pandemic began. And now, as so much of life looks like it did before the pandemic, it’s reasonable to wonder: is it over? It sure seems like it — even the president said so in September, and COVID precautions are barely seen in some locales.
Still, we continue to have thousands of new COVID-19 infections and hundreds of related deaths in this country each day. So, is it truly over? And what changes if that determination is ever formally made?
Defining a pandemic’s start is tricky; the same goes for its end
When the pandemic began, I thought declaring an end would be straightforward: experts would count up conditions that marked a starting line, and once those conditions evaporated the pandemic officially would be over.
Unfortunately, it’s not that easy.
As strange as it may seem, there is no single, agreed-upon definition of pandemic that all countries, public health agencies, and world leaders use.
The word itself comes from the Greek words pan (meaning all) and demos (meaning people), which makes sense: a key feature of a pandemic is that it can affect just about everyone. More common definitions include:
an outbreak of a disease that occurs over a wide geographic area (multiple countries or continents) and typically affects a significant proportion of the population (Merriam-Webster Medical Dictionary)
a sudden outbreak that becomes widespread and affects a whole region, a continent, or the world due to a susceptible population (MedicineNet.com)
a disease prevalent throughout an entire country, continent, or the whole world (dictionary.com)
These standard definitions aren’t particularly specific; what, exactly, does “multiple countries” or “a whole region” mean? How prevalent (widespread) does a disease have to be to be considered a pandemic?
And even if we could all agree on its definition, no single person, government agency, or public health organization has the authority to declare that a pandemic has begun or ended.
Moving from pandemic panic to endemic acceptance
Some people have suggested a pandemic is over when everyone is behaving as though it is: no more precautions, restrictions, or changes in behavior compared with the period of time before these started. But if that’s true, people growing weary of restrictions, or those skeptical about their value, could ignore recommendations and create the impression that the pandemic is over — even as significant numbers of daily cases and deaths continue in the US and worldwide. That seems to be where we are with COVID right now.
Many pandemics eventually become endemic, meaning the infection is still present in a region or population but its behavior is predictable and the numbers of cases and deaths no longer spike. Learning to live with a virus is a key feature of an endemic virus; think flu or even the common cold. But it’s probably true that the transition from pandemic to endemic can only be recognized after it happens.
What to do until the COVID pandemic is clearly behind us?
Perhaps setting a firm end date on this pandemic doesn’t matter, anyway. What matters most is the number of ongoing infections, suffering and death, and the measures we should take to avoid infection. No one can say whether the coming winter months will bring a decline in infections, a continuation of the current situation (with hundreds of deaths and thousands of new infections each day in the US), or a spike in illness and death as more people are inside with relaxed precautions.
Common sense precautions still make sense, including these:
Wear a well-fitted mask in higher-risk settings (such as traveling in crowded conditions, crowded indoor settings, or on public transportation). Just because masking is no longer required doesn’t make throwing out your masks a good idea.
Isolate yourself if you test positive for COVID-19 (or if you have symptoms of COVID-19 and haven’t been tested yet). Contact a doctor to decide whether you should take antiviral treatment if you test positive for COVID-19.
The bottom line
It’s possible that experts will agree one day on a standard definition of “pandemic” and how to mark its arrival and departure. Already, policies regarding the pandemic (including financial assistance), and efforts to increase vaccination acceptance, are complicated by suggestions we’re past the pandemic when we’re actually not.
There’s a lot that’s still uncertain about the COVID-19 pandemic. Unfortunately, one thing seems clear: we can’t call it fully over yet.
Natural approaches to lowering high blood pressure can work better than drugs because you’re treating the underlying cause, and can end up having only good side effects.
The number one killer in the United States and on the planet Earth is a bad diet. (That is why I’ve dedicated my life to the study of nutrition.) Killer #2 is high blood pressure. The reason it’s so deadly is that it increases your risk of dying from so many different diseases: heart disease and stroke, to heart and kidney failure.
We’re talking an exponential increase in risk of dying from a stroke as our pressures go up, starting from around 110 over 70, an exponential increase in the risk of dying from heart disease, again starting at a blood pressure of about 110/70. We used to consider a blood pressure as high as 175 to be normal––normal if you wanted to die from the normal diseases, like heart attack and stroke. A “normal” of 175 over 110 could put you at over a thousand percent higher risk of having you croak from a stroke compared to the ideal—not the normal, but the ideal, which is down around 110/70.
The definition of high blood pressure, hypertension, dropped from as high as 190/110 down to 160/95, with treatment thresholds for high-risk groups starting at 150/90 down to 140/90, and then, most recently, 130/80. Now…instead of one in three Americans having hypertension, with the new definition, it’s closer to one in two, or more like two-thirds among those over the age of 45. Every time the threshold drops, labeling tens of millions more people as diseased, there’s this backlash. Same thing every time the cholesterol guidelines get more and more stringent; but don’t blame the guidelines. Americans are diseased. That’s the real problem. The American way of life is the problem, not the guidelines.
Maybe we should focus on that instead.
After all, the number one killer of American men and women is heart disease, a disease that can be prevented, arrested, and reversed with a healthy-enough diet.
So, even though a cholesterol of 200 may be normal, maybe we should tell people to strive for under 150. Even though a BMI of 24.9 is technically not overweight, an average height woman, for example, would be better off down around 120 pounds than 145. And, similarly, though a blood pressure of 120/80 may be normal, 110 would be a better top number, and 70 a better lower number, as even down in that range between 70 to 75, or 75 to 80, each 5-point increment is associated with a third more stroke, and at least a fifth more heart disease.
So, why are the new guidelines up at 130 over 80? With an average of three different blood-pressure drugs, you can force people’s blood pressures from 140 down to 120, compared to just giving them two blood-pressure drugs, and high-risk people live longer because of it. Significantly less death in the intensive treatment group, but, because of the higher doses and drugs, had more side effects. So, you have to weigh the risks versus benefits…
One to 2% of people on the drugs for five years will benefit, not having a cardiovascular event when they otherwise might have, and that has to be balanced against the higher risk of adverse side effects. So, you’ll hear commentators saying things like, yeah, the drugs decreased your risk of “events” by 25%, but increased your risk of a serious side effect by 88%. Okay, but those events can include things like death, whereas the side effects are more on the order of fainting.
“These adverse events [do] need to be weighed against the benefits with respect to cardiovascular events and death that are associated with intensive control of systolic blood pressure.” Like, if we use drugs to push high-risk people down to a top number of 120, we might prevent over 100,000 deaths and 46,000 cases of heart failure every year, but could cause “43,000 cases of electrolyte abnormalities and 88,000 cases of acute kidney injury.” Not great, but better than dying.
So, you can see the conundrum guidelines committees are in. On one hand, lowering blood pressure is good for your heart, kidneys, and brain, but at a certain point the side effects from the drugs could outweigh the benefits. Ideally, we want to get patients’ blood pressures as low as possible, but only want to use drugs to do it “when the effects of treatment are likely to be less destructive than the elevated blood pressure.”
The problem is that most people who die from heart disease, heart failure, and stroke may be in that borderline range not sufficiently elevated to warrant drug treatment.
If only there were some way to lower blood pressures without drugs to get the best of both worlds. Thankfully, there are. Regular aerobic exercise, weight loss, smoking cessation, increased dietary fiber intake, decreased alcoholic beverage intake, consumption of a more plant-based diet, and cutting down on salt. The advantage is, first of all, no bad side effects. Some lifestyle interventions can actually work better than drugs, because you’re treating the cause, and actually have instead good side effects. So, not 1 or 2% benefit over five years—everybody benefits.
Life has been on a steady downward slope for Hannah Camp Johnson, an intelligent, once-healthy 26-year-old woman from Alabama.
In August 2020, she contracted COVID-19. She experienced severe symptoms, including coughing, fever, and crippling fatigue; her oxygen levels fell, and she needed to take breathing medicine. She lost her ability to walk due to muscle loss in her legs.
Johnson experienced a brief recovery after two weeks of staying at home. She felt that she was getting better; her mobility improved, and she learned to walk again.
“I was walking fine. I was even doing swimming days where I would go down to the pool [at] my apartment and work out my legs with that. I would [also] go to a bookstore,” said Johnson, who has had a lifelong love of reading.
These improvements lasted for two months, then she started to fall sick again, and this time, she has yet to get better.
From 2020 to 2021, Johnson’s fatigue and cognitive problems worsened.
She could not walk without feeling winded and experienced palpitations and a rapid rise in heart rate every time she stood up.
Johnson previously had only hypothyroidism, which was under control, but six months after contracting COVID, her teeth started to deteriorate, and she was diagnosed with type 2 diabetes.
Her vision also began to decline rapidly, and she was prescribed her first pair of glasses in June 2021.
At around the same time she started experiencing an immense head pressure as if someone was gripping her brain.
Only three months after, Johnson was given an explanation for the gripping sensation.
She was diagnosed with having focal seizures and encephalitis (a form of neuroinflammation) on an electroencephalogram. Her seizures, which have gradually manifested to the surface have been a major contributor to her disability, Johnson told The Epoch Times.
Some people suffering from vaccine injuries have also experienced similar symptoms, but Johnson developed long COVID before vaccinations were available. By the time she was vaccinated in November 2021, she had already developed all of the above symptoms; the vaccine did not significantly improve her symptoms.
Johnson’s severe case of long COVID is not isolated.
The Main Cause of Long COVID Might Be Inflammation
Clinicians have yet to settle on the cause of long COVID. The disease is complicated and systemic; patients often present with a cluster of symptoms.
Specialists are familiar with and trained in different fields, bringing varied perspectives to the discussion about long COVID.
At the molecular level, studies point to remnant viral spike protein (1, 2) contributing to long COVID. The spike protein sits on the surface of COVID-19 viruses and binds to cell receptors such as angiotensin-converting enzyme 2 (ACE2) to help the virus infect the cell.
Though the virus can persist in the body— a study led by Dr. Sabine Hazan, gastroenterologist and CEO of Progenabiome, found the whole genetic sequence of the virus present in the stools up to a month after infection—the spike protein seems to persist for even longer.
A study led by pathologist Dr. Bruce Patterson, founder and CEO of the molecular diagnostic company Incelldx, found spike protein in the immune cells of long COVID patients 15 months after infection.
The spike protein contributes to various pathologies, such as inflammation (1, 2, 3).
Patterson and internal medicine physician Dr. Jessica Peatross hypothesize that a significant driver behind long COVID is inflammation of the inner lining of the blood vessels, also known as endotheliitis.
Spike proteins have been shown to cause damage to endothelial cells. Endothelial cells form the inner lining of all blood vessels; damage to these cells elevates the risk of systemic disease. Endothelial damage is believed to be the primary driver of severe COVID.
Patterson’s study also found the spike proteins were located in monocyte cells that patrol blood vessels as part of their function. When inflamed, monocytes can adhere to blood vessel walls and cause systemic blood vessel inflammation and damage (1, 2).
Spike protein could also be a reason behind the neurocognitive and neuropsychiatric symptoms in long COVID patients.
While the SARS-CoV-2 virus is too big to cross the blood-brain barrier that protects the brain from toxins in the blood, spike protein is small enough to cross. A study showed that the spike protein could cross the barrier in mice’s brains. A laboratory study tested spike protein using human cells on an artificially made blood-brain barrier. Researchers found that the protein could disrupt the barrier, perhaps compromising its ability to block out toxins.
With long COVID, other changes are occurring in the body.
Hazan said that she would find COVID-19 RNA in the stools of long COVID patients who tested at her laboratory. The microflora of these patients were also in a state of imbalance, also known as dysbiosis.
Gut dysbiosis can cause a leaky gut: the gut barrier becomes compromised, and the gut bacteria can cross the barrier into the body and its fluids. Though the gut can tolerate hosting billions of foreign organisms, other areas of the body recognize them as foreign invaders.
This causes immune cells to mount an attack against these bacteria, leading to inflammation.
“The virus itself is not an autoimmune disease, but triggers autoimmune inflammation,” said psychiatrist Dr. Adonis Sfera, “in which the body attacks itself.”
Current Ways to Diagnose Long COVID
Without a concrete and approved diagnostic test, clinicians have yet to reach a consensus on what defines long COVID. Most have relied on the patient’s physical examination and medical history to reach a diagnosis.
However, Patterson, by conducting blood tests on 250 patients with acute or long COVID, identified 14 markers that are commonly elevated in patients reporting long COVID symptoms.
Patterson’s company, Incelldx, sells a COVID testing kit that evaluates and analyzes the 14 cytokine levels to diagnose patients with long COVID.
This analysis is essential in differentiating long COVID from other diseases with similar symptoms. Patterson’s studies found that some people diagnosed with long COVID may actually be suffering from an acute COVID infection, post-vaccine injuries, re-activated fibromyalgia, or Lyme disease. Patterson’s studies uncovered different patterns in the elevation of the 14 cytokines related to the various conditions (1, 2).
Patterson’s research and subsequent studies have shown that the five most relevant cytokines for assessing long COVID differ from those associated with Lyme disease.
In diagnosing long COVID, distinguishing from other diseases would allow clinicians to give the most targeted treatment. “It’s absolutely critical in terms of treatment. Lyme patients, maybe they need additional antibiotics; for ME-CFS (myalgic encephalomyelitis-chronic fatigue syndrome), maybe they need Valtrex or anti-herpes medication in addition to the immune modulators that we use—it is absolutely critical,” Patterson said.
When cytokine in the blood rises too quickly, a cytokine storm is triggered, associated with an increased risk of severe disease outcomes and death.
Cytokines are specialized for different functions in the body and are a signal of immune and inflammatory activity.
Therefore, physicians like Dr. Jeffrey Nordella, who follows Patterson’s cytokine panel, reason that a person’s symptoms can all be related to cytokine levels.
Other clinicians have argued that while the panel is helpful, it may not give the full perspective in a diagnosis.
Peatross, who has given up her medical license due to limitations placed on her license for approving vaccine exemptions, told The Epoch Times that talking to a patient is her primary strategy, and blood tests that look at cytokine levels and iron augment the overall diagnosis.
Since cytokines are a sign of an immune response, individuals with a compromised immune system through drug suppression or poor health may not exhibit such high levels of the cytokines, said Peatross.
Therefore, clinicians focus on the patient’s symptoms and watch for symptom clusters typically associated with long COVID.
Common symptoms include fatigue, brain fog, shortness of breath, and rapid heart rate.
“When you get people talking about brain fog, then you think of long COVID,” said critical care specialist Dr. Paul Marik.
Yet Mary Lee, who has been suffering from long COVID since Dec. 2021, said that words such as “fatigue” and “brain fog” do not adequately describe her physical tribulations.
Fatigue
One of the most common and debilitating symptoms of long COVID is fatigue.
A 2021 study led by Patterson demonstrated that over 30 percent of the long COVID patients going through his program reported fatigue as a significant symptom. Another study has shown that 80 percent of people with long COVID report fatigue.
Johnson described chronic fatigue as “living with limited numbers of batteries” and long COVID patients needing to plan their days accordingly.
“Throughout the day, I run out of units of energy, and I only have so many units of energy to give. Before I know it, I’m completely unable to function,” she said.
Tiffany Braccia, aged 59, has lived with COVID symptoms since April 2020. She needs to rest before partaking in any activity and must make sure that she doesn’t spend all of her energy on one thing.
If long COVID patients overspend their energy, they could be exhausted for days.
Justin Wilhites, aged 42, developed COVID symptoms in 2020 and has never recovered. He told The Epoch Times that there were good days and bad days, and he could tell which type of day he would experience the minute he woke up. For many long COVID patients, the bad days mean very little activity except hoping that the next day will be better.
Sometimes fatigue can worsen; Johnson and Wilhites each said they had seen a clear decline in their energy over the two years.
Wilhites described the decline as gradual steps down.
For a while, symptoms such as fatigue would appear to stabilize and form the new normal. Then he would experience a deterioration that would stabilize before falling again.
“It’s like steps down,” said Wilhites, “goes normal, and then it goes down.”
Mitochondria, a membrane-enclosed cellular organelles, which produce energy, 3D illustration.
Cognitive Problems
Besides fatigue, another concerning and hugely debilitating symptom is cognitive decline, colloquially described as brain fog.
A UK study found that around 70 percent of COVID patients report problems with concentration and memory after contracting COVID.
Brain fog is described as confusion, lack of mental clarity, and forgetfulness; in long COVID patients, the symptoms are typically problems with memory and concentration.
Brain fog not only impacts long haulers’ professional ability but also can affect day-to-day skills such as being able to drive, dressing, and maintaining basic hygiene.
Braccia said that several weeks after her COVID infection in March, she suddenly lost her grooming abilities; she did not know how to shower or use shampoo. That period was particularly dark and despairing.
She has since developed coping mechanisms to remember instructions, but for some time, she could not remember even two-step instructions.
The inability to concentrate due to brain fog can affect hobbies such as reading and watching movies.
Johnson has given up reading after a progressive decline in concentration and memory.
After reading, she would need to go online to search for summaries and analyses of the works “because I would have already forgotten what I’ve already read,” said Johnson, “I had a whole bookshelf full of my books, and I just can’t even pick them up anymore.”
Despite being only in her mid-20s, Johnson has been documented as appearing with dementia symptoms; words like “amnesia” have been recorded in her medical histories.
Memory loss depletes long haulers’ vocabulary. Johnson, who used to pride herself on her eloquence, began to notice that she would sometimes need help finishing her sentences.
Braccia said that in stressful situations, words would escape her.
Stuttering or slurring may also creep into sentences, said Wilhites. Depending on the person, socializing could go from stressful to infuriating.
Another consequence of brain fog is difficulty keeping up with conversations or understanding nuances.
Braccia said that she would easily become so fixated on what she would say that she missed social cues, only to notice them a few moments later.
“I’m always three seconds behind everyone else,” she said.
Muscle Weakness and Pain
Around 20 percent of long COVID patients report muscle pain, which often appears as an early symptom. Weakness, as an association with fatigue, has been reported in 60 percent of long COVID patients.
“My muscles are like jelly,” said Wilhites, describing his constant state of weakness.
Since April 2020, Wilhites has been in constant pain across the muscles in his back and neck and can barely walk due to the pain.
“It would hurt me to hug you; my back muscles, my shoulder muscles, my biceps, my triceps, anything that’s involved in a hug hurts me,” said Wilhites, “And that’s still to this day.”
Braccia experienced a sudden weight gain a few months after contracting COVID. Though she lost the weight a few months later, she was left with persistent weakness in her joints and legs.
Muscle pain and shooting neuropathic pain have also been persistent for her, confining her to inactivity.
Arm weakness
Shortness of Breath and Tachycardia
Shortness of breath can be due to pulmonary causes and cardiac problems, including tachycardia, a rapid heart rate of over 100 beats per minute (bpm).
Research has revealed that 26 to 51 percent of COVID patients have experienced persistent shortness of breath, also known as dyspnea. A 2021 study found that 25 to 50 percent of long COVID patients reported “persistent tachycardia or palpitations.”
Symptoms such as brain fog, fatigue, muscle weakness and pain, and tachycardia are also seen in other conditions, including Lyme disease and chronic fatigue, but shortness of breath is one of the hallmarks of COVID-related chronic diseases.
Shortness of breath is attributed to fatigue and post-exertional malaise and can be episodic or constant.
For Wilhites, just walking up and down the stairs would be enough to leave his breathing shallow and make him feel as if he was about to faint.
Tachycardia can often cause shortness of breath as once the heart beats too fast, there may not be enough oxygen being released into the body.
“I’ve tested it and even showed my primary care. My heart [when] I’m sitting down can be like 80 [bpm], and then I stand up, and it just jumps to at least like 125,” she said.
Johnson told The Epoch Times on Dec. 17, 2022, that her heart rate can now easily reach 210 beats per minute when she stands up.
Prolonged shortness of breath
Mental Health
Perhaps one of the least discussed effects of long COVID is its detrimental impact on people’s mental health. The severity of its impact appears to be particularly significant in patients suffering from long COVID for an extended period.
Johnson was diagnosed with post-traumatic stress disorder (PTSD) from a previous event, but since Feb. 2021, she has been battling PTSD from COVID-19 and its complications.
Lee described that it is similar to having your life robbed away.
Many long haulers were previously healthy and strong. Passing every day by lying in bed and being unable to enjoy many of their interests can be difficult to accept without receding into despair.
Suicidality is a great risk for long COVID patients, as pointed out in a 2021 paper by Leo Sher that discussed prevalent mental health problems in long haulers.
Sher wrote that mental health problems such as PTSD, anxiety, and psychosis may be caused by damage to the brain from the infection or can result from the experience of the disease.
The decline in quality of life and losing hope of recovery appear to be major factors behind the mental health crisis.
Johnson has noticed a definite decline in her health, her fatigue has gotten worse, and it seems to her that she is developing a new symptom every few months.
Wilhites’s wife said that many doctors focus on treating his symptoms rather than addressing the cause of his illness. Medication relieves his symptoms but is only a temporary fix.
His body soon gets used to the drugs, and the symptoms resurface; at the same time, a new symptom appears and is suppressed temporarily with medication.
Wilhite’s health and quality of life are on a gradual but certain decline.
Braccia related that it is like living to pass the day.
“It’s a very sad existence,” she said, “I wouldn’t recommend it for anybody.”
Both Johnson and Braccia have started counseling and developed support systems.
Lee, a person of faith, told The Epoch Times that this physical tribulation has allowed her to re-evaluate what really matters to her in life, and some things she once held onto no longer mattered as much.
Believing that nothing happens in life without a reason, Lee said that she has been journaling every day about what she is grateful for, and it has given her a new perspective on her life and her relationships with people.
She said her spiritual journey was probably the most important part of the past year of living with long COVID.
Although the general understanding of long COVID has improved in the past year, many questions about the persistent sequelae experienced by some people after an acute SARS-CoV-2 infection remain, according to experts.
“Initially, people assumed this was only brain fog and fatigue, but now, in this last year, a slew of issues related to long COVID have emerged,” Ziyad Al-Aly, MD, FASN, chief of the research and development service at the Veterans Affairs Saint Louis Health Care System, told Healio. “This includes neurologic and mental health disorders, heart and cardiovascular conditions, increased risk of diabetes, and so on.”
One recent study assessing data published through March 2022 found that the global estimated pooled prevalence of long COVID-19 was “substantial” at 43% — equal to approximately 200 million people who have had post-COVID-19 health consequences, the researchers reported.
Another study found that nearly 6% of children who tested positive for SARS-CoV-2 after seeking care at an ED reported lasting effects from their infection, 10% of whom were hospitalized for the condition.
Helping patients with long COVID has not been simple.
“Early in the pandemic, most people had not heard of long COVID, so a major focus was on validating those experiencing such symptoms and educating others,” Brian L. Block, MD, assistant professor of medicine in the division of pulmonary and critical care at the University of California, San Francisco, told Healio. “Thankfully, long COVID is now more broadly known, but understanding how and why it develops remains elusive.”
‘A combination of similar syndromes’
In October 2021, WHO published a clinical case definition of long COVID that says the condition “occurs in individuals with a history of probable or confirmed SARS-CoV-2 infection, usually 3 months from the onset of COVID-19 with symptoms that last for at least 2 months and cannot be explained by an alternative diagnosis.”
According to WHO, the most common symptoms include fatigue, shortness of breath and cognitive dysfunction, plus others that can generally have an impact on everyday functioning.
The CDC considers a patient to have long COVID — it generally uses the term “post-COVID conditions” — if symptoms persist 4 weeks after the acute phase of illness, although it notes that “many patients continue to recover between 4 and 12 weeks.”
“Although standardized case definitions are still being developed,” the CDC says, “in the broadest sense, post-COVID conditions can be considered a lack of return to a usual state of health following acute COVID-19 illness. Post-COVID conditions might also include development of new or recurrent symptoms or unmasking of a pre-existing condition that occurs after the symptoms of acute COVID-19 illness have resolved.”
Researchers in the United Kingdom developed a novel tool called the Symptom Burden Questionnaire for Long COVID, a patient-reported outcome measure that was created using data from 13 patients but was then field tested by 274 adults with long COVID. The researchers determined it was accurate, made it available for clinicians and researchers worldwide and said it can assess the symptoms of long COVID and help deliver clinical care.
In addition to pinpointing symptoms, researchers have begun determining what pre-existing conditions contribute to the possibility of developing long COVID.
One study found that pre-existing type 2 diabetes, SARS-CoV-2 RNA in the blood, Epstein-Barr virus DNA in the blood and the presence of certain autoantibodies could anticipate a patient developing long COVID. The study showed the autoantibodies decreased protective SARS-CoV-2 antibodies as they themselves increased, suggesting a relationship between long COVID, autoantibodies and an elevated risk for reinfection.
“It remains hard to predict which people will have more persistent symptoms of long COVID, and which will have a better trajectory. I think some of this is because what we have been calling long COVID — as if it is just one disease with one mechanism and one expected outcome — is actually a combination of similar syndromes, each of which may have its own cause, expected trajectory, and outcome,” Block said.
“Having more granularity about long COVID, such as being able to say a person has a certain subtype, will make it easier to predict what will happen to a certain patient, and tailor treatments appropriately,” he said.
One thing experts know for certain is that caring for patients with long COVID requires a collaborative effort.
“Patients with long COVID continue to benefit from a multidisciplinary approach where they can see a physician with expertise in the symptoms they are feeling, along with critical team members such as a physical therapist, psychiatrist, social worker, and others for support,” Block said.
Strain on public health
Unfortunately, such care is “resource intensive” and not always available as the health care system continues to experience strain, Block added.
“It’s not an understatement to say the U.S. health care system was stretched thin by the COVID-19 pandemic,” Sandra Adamson Fryhofer, MD, chair of the AMA board of trusteesand member of the CDC’s Advisory Committee on Immunization Practices COVID-19 vaccines work group, told Healio.
Sandra Adamson Fryhofer, MD
“From personal protective equipment shortages and constant battling against misinformation to significant physician burnout, physicians have been asked to do more with less for nearly 3 years,” Fryhofer said.
She said physician shortages were projected to be severe even before COVID-19, and the U.S. is now approaching a public health emergency. How much long COVID is contributing to the strain on health care services compared with other “surging” illnesses is up for debate, Al-Aly said.
“At this point, it’s really hard to disentangle the strain that the health system is experiencing and how much is really due to the influx of patients with long COVID vs. other things,” he said. “I can tell you, anecdotally, if you go to any post-COVID clinic or any COVID clinic, the wait time is unacceptably long.”
Al-Aly explained that if patients go online or call to set up an appointment at a long COVID clinic, they would be lucky to get an appointment within 3 or 4 months.
“There is really a mismatch between demand and capacity, or the ability to provide services,” he said.
Compounding the problem of physician shortages and long patient waits is that fact that no guidelines or official means of diagnosis have been established.
“As is the case in a lot of diagnoses, diagnosing long COVID is often a process of elimination,” Fryhofer explained. “It shows up both in patients who were very sick from COVID and patients who had no symptoms at all. It can show up immediately or months after infection. If a patient had no symptoms before and now has new symptoms, a physician cannot simply label it as long COVID without first ruling out other conditions.”
This extra guesswork can prolong the treatment and care process, creating heavier workloads for doctors and longer waits for patients, which could be detrimental as other public health emergencies emerge.
Aaron E. Glatt, MD
“The U.S. health care system is a very strong system, but it’s breaking in a lot of places,” Aaron E. Glatt, MD, chairman of the department of medicine and chief of infectious diseases at Mount Sinai South Nassau in Oceanside, New York, told Healio.
Glatt listed some infectious diseases that are eating up public health resources in the U.S — COVID-19, monkeypox and influenza among them. Glatt practices in one of the New York counties where poliovirus has been detected in wastewater.
“You’re not catching long COVID from somebody else, so there’s a little bit less of a public health urgency — but that doesn’t mean it’s not an urgent, real concern for the patients who have to deal with this every day,” Glatt said. “Unfortunately, when you’re dealing with debating where we should put limited resources, it is not always easy to give every disease the right funding it needs to solve the issues it presents.”
Treatments? ‘It’s still zero’
There remain no specific treatments for long COVID — and that is not surprising, Al-Aly said.
“If you asked me a year ago for the number of approved therapeutics for long COVID, I would have said zero. And guess what? It’s still zero,” said Al-Aly, who called the lack of treatments “a major deficiency.”
“We really need to promote awareness [of this],” he said. “This is really a sore point. People are hurting with long COVID … and they want treatment yesterday.”
Block said that some centers appear to have standardized treatment protocols that they use for all patients with long COVID, which can range from prescription medications that have been repurposed for long COVID to supplements, recommendations about dietary changes and other protocols.
However, he said, this is not the same at all facilities, including his own.
“At our clinic we do not employ this practice, given our belief that each patient with long COVID requires an individualized treatment plan and given that the evidence base for many of the offered treatments is thin,” he said.
Glatt said there is not really a need to develop a protocol to apply to patients with long COVID.
“If you’re dealing with, let’s say for argument’s sake, shortness of breath, pulmonary and cardiac complications — a generalized protocol [for that] might be inappropriate for someone dealing with loss of smell or people who are fatigued,” he said. “I don’t think it’s a one-size-fits-all protocol.”
According to Glatt, a lot of clinicians treating patients with long COVID are really just monitoring them and gathering data, which is still very important.
“Everybody wants to hear ‘treatment,’ but sometimes the first step is understanding what’s going on and then, once you understand, maybe you have a chance to treat,” Glatt said.
He said long COVID is like other illnesses that are poorly understood — chronic fatigue, for example — making treatment difficult. The first and foremost thing to remember when initiating care and treatment for any illness, including long COVID, is to try to make the patient feel better, Glatt said.
“That’s why we became doctors,” he said. “I may not understand why they have fatigue or shortness of breath, but what can I do to make them feel better? I may not have the pills to make this go away in 5 days, but I can be both a compassionate and sympathetic person and figure out, with the patient, how they can normalize their life.”
Getting the lives of patients with long COVID back to normal is crucial to their mental health because many have an increased risk for depression and depressive symptoms, as well as other mood disorders, studies have shown.
“One question we get in clinic is whether a patient can and should return to work, or an employer may send us disability paperwork to complete,” Block explained. “With a new disease of uncertain pathophysiology and trajectory and limited objective testing, it can be very difficult to prognosticate or make informed decisions about what level of activity is safe.”
This may complicate the decision-making process for people with long COVID and those treating them.
“Considerations include the tradeoff between having more time to rest — when we know some people with long COVID feel worse when they overexert themselves — vs. losing the sense of meaning that can come from work, potentially contributing to a sense of loss or other mood disorder, which can magnify the symptoms of long COVID,” Block said.
Preventing COVID is preventing long COVID
Experts agree that preventing COVID-19 altogether is the key to lessening the burden of long COVID.
“I tell people the best way to not get long COVID is to not get COVID,” Glatt said. “People who are especially at higher risk for serious COVID should be very careful in terms of making sure that they’re fully vaccinated and boosted.”
It is also important to acknowledge that studies have shown that vaccination may not fully protect people from long COVID symptoms if they experience a breakthrough infection.
A study by Al-Aly and colleagues that was published in Nature Medicinein June assessed nearly 34,000 vaccinated patients with breakthrough SARS-CoV-2 infections and found that they had a higher risk for long COVID (HR = 1.5; 95% CI, 1.46-1.54) compared with almost 5 million contemporary controls with no documented infection.
Compared with unvaccinated patients with a SARS-CoV-2 infection, patients with a breakthrough infection had a 34% lower risk for death (HR = 0.66; 95% CI, 0.58-0.74) and a 15% lower risk for incident long COVID (HR = 0.85; 95% CI, 0.82-0.89).
At the time the study was published, Al-Aly said the data showed vaccines “reduce but do not eliminate” the risk of long COVID and called them “an imperfect shield.”
“With every infection, one’s odds of getting long COVID increases,” Fryhofer said. “This is what it’s like to live during a pandemic.”
Fryhofer added that the COVID-19 vaccines are “exceptionally effective at preventing severe disease and death,” but despite this, some communities and segments of the population — particularly children — lag far behind on vaccination rates, especially boosters.
“The new bivalent vaccine is specifically effective at combating the two most dominant strains of COVID circulating today, and I urge everyone to get it as soon as you’re eligible,” she said.
‘The even bigger riddle’
SARS-CoV-2 is not the first virus to cause lasting effects in previously infected people
“Long COVID improved our awareness that viruses produce long-term consequences,” Al-Aly said. “In the U.S., SARS-CoV-2 is the biggest example, or the most vivid one out there now, to help us understand that infections and viruses [can have lifelong consequences]. In most of the public consciousness, and even in the medical field, people used to regard them as acute events that you can turn the page and move on from as if nothing happened.”
The magnitude of SARS-CoV-2 and its long-term effects has also led to more funding for the study of post-viral conditions.
“This is really important,” Al-Aly said, “not just to solve the problem of long COVID alone, but to solve the even bigger riddle of the post-viral condition to help us address other problems that people have been suffering from for years and decades.”
Block agreed, suggesting that because COVID-19 was a “monumental global event,” long COVID has received more attention and research funding than other post-viral syndromes that preceded it. However, he cautioned that the attention that was given to COVID-19 is waning.
“In the past year, the degree of societal concern about acute COVID has decreased substantially,” Block said. “With this return to normalcy, people experiencing long COVID may feel left behind and marginalized as society ‘moves on’ and they continue to feel sick.”
He said that as COVID “loosens its grip on our collective attention,” people experiencing long COVID may find — like people with other presumed post-viral syndromes — that the attention and support they had has dried up.
Known as the City of Hope patient, he is the fourth patient in the world and the oldest to go into long-term remission of HIV without antiretroviral therapy (ART) for over a year after receiving stem cells from a donor with a rare genetic mutation. He is now 66 years old. He was 63 when he received the transplant.
Among those patients, he also had HIV the longest, since 1988, before going into remission for HIV and leukemia.
Patient’s case opens up opportunities for older patients living with HIV and a blood cancer to receive a transplant and achieve remission for both diseases if a donor with rare genetic mutation can be identified.
Research presented today at AIDS 2022 press conference, highlighting the latest HIV research.
City of Hope is a global leader in stem cell transplantation for patients with blood cancers and patients with HIV/blood cancer.
LOS ANGELES — City of Hope, one of the largest cancer research and treatment organizations in the United States, announced today that a 66-year-old man who was diagnosed with HIV in 1988 has been in remission of the virus for over 17 months after stopping antiretroviral therapy (ART) for the disease following a stem cell transplant from an unrelated donor for leukemia, according to research presented today at the AIDS 2022 press conference by Jana K. Dickter, M.D., City of Hope associate clinical professor in the Division of Infectious Diseases. He received the transplant nearly 3 1/2 years ago at City of Hope.
The man, known as the City of Hope patient, lived with HIV for over 31 years, the longest of any of the three previous patients with HIV who have gone into remission for a blood cancer and HIV. He was 63 years old when he received a transplant, the oldest patient to receive a transplant and go into remission for HIV and leukemia.
The patient received a chemotherapy-based, reduced-intensity transplant regimen prior to his transplant that was developed by City of Hope and other transplant programs for treatment of older patients with blood cancers. Reduced-intensity chemotherapy makes the transplant more tolerable for older patients and reduces the potential for transplant-related complications from the procedure.
The patient received a blood stem cell transplant at City of Hope in early 2019 for acute myelogenous leukemia from an unrelated donor who has a rare genetic mutation, homozygous CCR5 Delta 32. That mutation makes people who have it resistant to acquiring HIV. CCR5 is a receptor on CD4+ immune cells, and HIV uses that receptor to enter and attack the immune system. But the CCR5 mutation blocks that pathway, which stops HIV from replicating.
The City of Hope patient has not shown any evidence of having replicating HIV virus since the transplant. He stopped taking ART for HIV in March 2021. He might have been able to stop the therapies sooner but wanted to wait until he was vaccinated against COVID-19.
“We are proud to have played a part in helping the City of Hope patient reach remission for both HIV and leukemia. It is humbling to know that our pioneering science in bone marrow and stem cell transplants, along with our pursuit of the best precision medicine in cancer, has helped transform this patient’s life,” said Robert Stone, president and CEO of City of Hope and the Helen and Morgan Chu Chief Executive Officer Distinguished Chair. “The entire team at City of Hope is honored to make a difference every day in the lives of people with cancer, diabetes and other life-threatening diseases.”
“We were thrilled to let him know that his HIV is in remission and he no longer needs to take antiretroviral therapy that he had been on for over 30 years,” Dickter said. “He saw many of his friends die from AIDS in the early days of the disease and faced so much stigma when he was diagnosed with HIV in 1988. But now, he can celebrate this medical milestone.”
“The City of Hope patient’s case, if the right donor can be identified, may open up the opportunity for more older patients living with HIV and blood cancers to receive a stem cell transplant and go into remission for both diseases,” Dickter added.
“When I was diagnosed with HIV in 1988, like many others, I thought it was a death sentence,” the man, who wishes not to be identified, said. “I never thought I would live to see the day that I no longer have HIV. City of Hope made that possible, and I am beyond grateful.”
City of Hope is a leader in treating patients with blood cancers, as well as patients with HIV and blood cancers with transplants. City of Hope has one of the nation’s leading transplant programs and is at the forefront of using transplants to treat older adults with blood cancers. The institution has performed nearly 18,000 transplants since 1976.
City of Hope was one of the first centers in the United States to perform effective, curative autologous transplants, which use a person’s own stem cells, for patients with HIV-related lymphoma. When many centers still treated patients with low-intensity, noncurative treatment approaches, City of Hope challenged that paradigm by demonstrating that autologous transplants could be used to cure patients with HIV-related lymphomas who would otherwise die.
City of Hope further pioneered the use of gene-modified blood stem cell transplants to evaluate the use of stem cells engineered to be resistant to HIV infection. The institution was also a primary national co-leader in two National Cancer Institute-sponsored trials for autologous as well as allogeneic stem cell transplantation, which use a donor’s stem cells, for patients with HIV and blood cancers. These trials led to a change to the national standards of care on how best to manage this vulnerable patient population.
Leveraging their expertise in cellular immunotherapy, City of Hope scientists have also developed chimeric antigen receptor (CAR) T cells that can target and kill HIV-infected cells and control HIV in preclinical research. They are working to start a clinical trial using CAR T cell therapy, which has the potential to provide HIV patients with a lifelong viral suppression without ART.
“The City of Hope patient is another major advancement. It demonstrates that research and clinical care developed and led at City of Hope are changing the meaning of an HIV diagnosis for patients across the United States and the world,” said John Zaia, M.D., Ph.D., director of City of Hope’s Center for Gene Therapy, Aaron D. Miller and Edith Miller Chair for Gene Therapy and a leader in HIV research. “City of Hope remains at the forefront of clinical research that changes people’s lives for the better.”
Under the care of City of Hope hematologist Ahmed Aribi, M.D., assistant professor in the Division of Leukemia, the patient received three different therapies to get him into remission before receiving a transplant. Most patients achieve remission after one therapy. The remission is necessary because a transplant is an intensive procedure that can cause serious complications.
For the transplant, Aribi and his team worked with City of Hope’s Unrelated Donor BMT Program — directed by Monzr M. Al Malki, M.D. — to find a donor who was a perfect match for the patient and had the rare genetic mutation, which is found in just 1-2% of the general population.
The patient did not experience serious medical issues after transplant.
“This patient had a high risk for relapsing from AML [acute myeloid leukemia], making his remission even more remarkable and highlighting how City of Hope provides excellent care treating complicated cases of AML and other blood cancers,” Aribi said.
A 66-year-old man is the oldest person yet to possibly be cured of HIV after undergoing a stem cell transplant, researchers announced Wednesday.
The man had HIV for more than 31 years when he received a blood stem cell transplant in early 2019 for acute myeloid leukemia (AML) using cells from a donor with a rare genetic mutation that prevents HIV from entering human cells, making people who have it resistant to most strains of the virus.
Dickter J, et al.
The man has remained free of replicating HIV since his transplant — including for the last 17 months after stopping treatment for HIV, said Jana K. Dickter, MD, a physician at City of Hope National Medical Center in Duarte, California, where the patient was treated. His leukemia also is in remission.
“This research is particularly important because people with HIV continue to live longer thanks to advances in antiretroviral therapy,” Dickter said during a press conference announcing the findings ahead of the AIDS 2022 meeting in Montreal.
She said the case “opens possibilities for other older persons living with HIV and blood cancer to receive a transplant and achieve remission from both diseases if a donor with this rare genetic mutation can be identified.”
At 63 years old when he underwent the procedure, the “City of Hope patient” — as he is being called — was the oldest person with HIV and leukemia to undergo a transplant and go into remission for both, according to Dickter and colleagues.
He is at least the fourth person to have potentially been cured of HIV after receiving stem cells from someone with the CCR5-delta 32 mutation, and the second such case to be made public this year.
In February, researchers at the Conference on Retroviruses and Opportunistic Infections (CROI) announced that, for the first time, a woman had achieved sustained treatment-free remission this way. The so-called “New York patient” was said to be in remission for more than a year without treatment.
Two other cases were announced in past years at CROI, including the “Berlin patient,” later identified as Timothy Ray Brown, who died in 2020 following a recurrence of AML. Brown remained HIV free for the rest of his life after undergoing a bone marrow transplant in 2007.
A man known as the “London patient” who later identified himself as Adam Castillejo was reported in 2020 to have been in HIV remission for 30 months after undergoing allogeneic hematopoietic stem cell transplantation for Hodgkin’s lymphoma.
Experts have warned that stem cell transplantation is too risky and expensive to be a conventional cure for HIV. What these cases have done, however, is prove that it is possible to cure HIV, a complex virus that can be suppressed to undetectable levels with potent medication but remains notoriously difficult to eliminate, experts have said.
“Although a transplant is not an option for more people with HIV, these cases are still interesting, still inspiring, and help illuminate the search for a cure,” Sharon Lewin, MBBS, PhD, president-elect of the International AIDS Society and director of The Peter Doherty Institute for Infection and Immunity in Melbourne, Australia, said during an earlier press briefing. Lewis was not involved in the case.
Before his transplant, the “City of Hope” patient had sustained an undetectable viral load on ART since the 1990s, according to Dickter and colleagues. He had HIV the longest of any of the four patients who have achieved long-term HIV remission via stem cell transplant.
He also received the least immunosuppressive regimen of any of them before his transplant. The regimen was designed for older and less-fit patients “to make transplantation more tolerable for them,” Dickter said.
“This patient’s outcome and the results of this research are profound,” Dickter said. “Because this patient was older, lived the longest with HIV prior to transplant and received the least immunosuppressive therapy compared to the previous patients who had achieved remission from HIV after stem cell transplantation, we now have evidence that some HIV patients with blood cancers may not need fully intensive immunosuppressive therapy prior to transplant in order to put them into remission.”
The man continued taking an ART regimen of emtricitabine, tenofovir alafenamide and dolutegravir for more than 2 years after his transplant, stopping in March 2021 after he was vaccinated against COVID-19.
References:
Dickter J, et al. Abstract 12508. Presented at: International AIDS Conference; July 27-Aug. 2, 2022; Montreal (hybrid meeting).
There have now been several cases of long-term HIV control following aggressive treatment of cancer diagnosed after HIV was suppressed by ART. Although the inability to detect HIV in these cases doesn’t prove that the infection has been truly cured, the longer these remissions are followed, the more likely a true sterilizing eradication or cure has been affected. Each of these cases is important, and we continue to hope that by studying them as a group, we might discover unifying evidence that enables us to find ways to the same end in larger numbers of cases without the toxicity and risk for mortality associated with cancer therapy and stem cell transplantation. The current case extends these previous reports and again used marrow donation from an individual carrying the delta CCR5-delta 32 mutation, which confers HIV infection resistance. We look forward to longer term follow-up of this case and of others that we hope to see over time. HIV cure remains a tremendous goal of a large and dedicated research community.
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